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Mycobacteria infection induced cascade of epigenetic alterations promote training in bystander macrophages

GSE278768 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 12 samples Submitted 2026/07/09 Platform GPL16791
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 12 samples

What it is
ChIP-seq / ATAC-seq (genome binding and open chromatin)Where proteins bind the genome, or which regions are open and active.
Organism
Homo sapiens (human)
Samples
12 samples: 6 conditions, mostly in duplicateGroups are read from the sample names, not from the paper. Check the list below.
Data you can get
A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Paper
Mycobacterium tuberculosis infection triggers IL-1β-dependent epigenetic training in bystander macrophagesmBio · 2026
Summary (written by the submitters)
Mycobacterium tuberculosis (Mtb) actively remodels host cell functions to promote its intracellular survival. Emerging evidence suggests that Mtb also significantly affects uninfected bystander cells within the host. However, the mechanisms underlying bystander cell modulation and their functional consequences during Mtb infection remain poorly understood.
Read the full summary ↓
In this study, we show that Mtb infection alters the host epigenome, resulting in correlated gene expression changes not only in infected cells but also in bystander cells. We demonstrate that cytokines secreted by Mtb-infected cells, particularly interleukin-1 beta (IL-1β), mediate these epigenetic changes in bystander cells, creating an intracellular environment similar to that of infected cells. These epigenetic alterations in bystander cells lead to population-wide trained immunity, enhancing the response of both infected and bystander cells to subsequent secondary stimuli. Our findings provide a mechanism for the propagation of trained immunity in a cell population and highlight bystander cells as active participants in shaping the innate immune response to Mtb infection. Understanding these intercellular communications presents a new frontier for developing comprehensive strategies that target both infected and bystander cells to modulate the broader cellular and immune response to tuberculosis.
Published in
Mycobacterium tuberculosis infection triggers IL-1β-dependent epigenetic training in bystander macrophages
Gulzar S-e-J, Umar I, Saravanan B et al. · mBio 2026 · PMID 42478839 · doi:10.1128/mbio.01214-26
This dataset
Open GSE278768 in finder → Find more human RNA-seq datasets →
Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

Series matrix ↓
2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE278768_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓
3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

Raw reads on ENA ↗

What the files usually look like: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1168865 and SRA study SRP536575. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 42478839) ↗
Study design
6 conditions, mostly in duplicate
THP1, Uninfected, RNA-seq, ×2 THP1, Infected, RNA-seq, ×2 THP1, Uninfected, H3K27ac, ChIP-seq, ×2 THP1, Infected, H3K27ac, ChIP-seq, ×2 THP1, Uninfected, PolII, ChIP-seq, ×2 THP1, Infected, PolII, ChIP-seq, ×2

Supports a between-group comparison across 12 samples.

How we read this: 6 replicated groups read from 12 sample titles; they account for 12 of them. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study
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